The Evolutionary Origins of Irreducible Complexity, Part 3

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May 17, 2012 Tags: Genetics

Dennis Venema. You can read more about what we believe here.

The Evolutionary Origins of Irreducible Complexity, Part 3

Note: One of the challenges for discussing evolution within evangelical Christian circles is that there is widespread confusion about how evolution actually works. In this (intermittent) series, I discuss aspects of evolution that are commonly misunderstood in the Christian community. In this post, we continue to examine the evidence that new genes can become part of “irreducibly complex” structures through gradual mechanisms.

In the previous post in this series we introduced the p24-2 gene, a brand-new gene identified in a large survey that compared several fruit fly (Drosophila) genomes to each other. The p24-2 gene stuck out like a sore thumb in this survey because it is present in only one fly species (Drosophila melanogaster). This gene arose from a duplication of a nearby gene (the Éclair gene) after D. melanogaster parted ways with other fly species within the last 3 million years. Pairs of recently duplicated genes and their “parent” genes are interesting to biologists studying how new gene functions arise—as well as an excellent opportunity to test the Intelligent Design (ID) argument from Irreducible Complexity (IC), as we discussed in the last post.

Éclair and p24-2 have distinct essential functions

The Éclair and p24-2 genes are part of a larger gene family in flies called p24 proteins. There are nine p24 protein genes in most Drosophila species, but the recent addition of p24-2 in D. melanogaster brings the total for this species to ten. The p24 protein family is a group of proteins that is widespread among diverse forms of life, such as plants, animals, and fungi. The various p24 proteins act as carriers for other proteins as they shuttle them from where they are made in the cell (the endoplasmic reticulum, or ER) to the Golgi apparatus (another location in the cell where proteins are modified and sorted). The p24 proteins do their jobs by binding their “cargo” proteins and loading them into small membrane spheres called vesicles that do the physical shuttling back and forth to different compartments within the cell.

Since p24-2 is a recent duplication of Éclair, the two genes are very similar at the structural level. Indeed, their amino acid sequences are nearly identical, as you might expect:

Of the 206 amino acids in each protein, only five differ between the two genes. (The figure above shows the amino acids for both genes using a single-letter code, and the differences are highlighted). Though these sequences are highly similar, already we see hints that the two genes are not equivalents. In fact, the difference between these two genes is already a little greater than the average difference we see between human and chimpanzee genes, and the separation of these two genes occurred much more recently than the human-chimpanzee split. Also, most of the differences are clustered at the one end of the protein, suggesting that a protein-protein binding domain has been altered. (See here for a description of binding regions that similarly latch onto sections of DNA)

Further work has confirmed the hypothesis that p24-2 and Éclair are not functionally equivalent genes. Several lines of evidence support this conclusion:

  1. Different defects are seen when the two genes are removed. While removing either gene usually results in the death of the fly, some rare flies do survive to adulthood. The survivors, however, have different defects: the loss of the Éclair gene results in female flies that cannot lay eggs, but loss of the p24-2 gene has no effect on egg laying at all.
  2. Éclair and p24-2 are not always found in the same cell types during development. For example, p24-2 protein is not found in the ovaries of adult females, whereas Éclair protein is very abundant in this tissue. This difference likely explains why removing Éclair is so detrimental to laying eggs, but removing p24-2 is of no consequence at all for egg laying.
  3. Éclair seems to share some functions with other p24 proteins that are less closely related to it than p24-2 is. For example, the “Basier” gene is found in all the same tissues in which Éclair is found. If a fly lacks Éclair, then it must have Basier (the flies all die if Basier is also removed). Similarly, when a fly lacks Basier, no loss of Éclair can be tolerated. These two genes work together and share their essential functions.
  4. One target “cargo” of Éclair has been identified - an important signaling protein called Wingless. The Wingless protein needs to be exported out of the cell in order to do its job, and without functional Éclair present, Wingless cannot make it from the ER to the Golgi, which it needs to do in order to be exported. The p24-2 protein, however, is completely dispensable for exporting Wingless. Thus p24-2 and Éclair are involved in transporting different cargo proteins. Éclair shares the function of exporting Wingless with another p24 family member (called Emp24), but not with its closer relative, p24-2.

In summary, while p24-2 and Éclair are both essential genes, they are involved with different essential functions. They transport different cargo proteins (in some cases in different tissues), and they show different defects when they are removed. While there is some sharing of function among p24 family members, Éclair shares with proteins other than p24-2.

Implications for the ID argument from IC

In our previous post we discussed ID proponent Michael Behe’s response to the 2010 paper that identified the new genes in Drosophila. In his response, Behe explained why he felt that paper was not a threat to the ID argument from IC:

I have never stated, nor do I think, that gene duplication and diversification cannot happen by Darwinian mechanisms, or that “they play almost no role at all” in the unfolding of life… What I don’t think can happen is that duplication/ divergence by Darwinian mechanisms can build new, complex interactive molecular machines or pathways…

It is also easy to conceive of a simple route to an “essential” duplicate gene that does little new. Suppose, for example, that some gene was duplicated. Although the duplication caused the organism to express more of the protein than was optimum, subsequent mutations in the promoter or protein sequence of one or both of the copies decreased the total activity of the protein to pre-duplication levels. Now, however, if one of the copies is deleted, there is not enough residual protein activity for the organism to survive. The new copy is now “essential”, although it does nothing that the original did not do.

We also discussed how Behe’s thoughts could be expressed as testable hypotheses:

If IC is correct, duplicated genes will not be part of new, complex molecular pathways or machines.

If IC is correct, duplicated genes that are both essential should “share” the original function.

As we can now see, these hypotheses have not been supported through additional work on Éclair and p24-2. We now do have good reason to think that p24-2 is involved in its own complex molecular pathway, and that it is not merely sharing an essential function with its parent gene Éclair. While we do not yet have all the details of how p24-2 and Éclair work, we already know that p24-2 performs its essential role without merely propping up the function of its parent gene. We also know that it carries a different cargo that Éclair is carries. It appears to have developed a new protein-protein interaction that allows it to carry something else. This role could not have been essential when it first arose, but it is essential now.

In summary, the evidence strongly suggests that the essential function of the p24-2 gene qualifies as IC in the ID sense, and that this IC function arose through an evolutionary process. Even if ID supporters quibble over the precise details of the Éclair/p24-2 story, the more important issue is one that is hopefully now abundantly clear: evolutionary processes can add new components to already complex molecular systems; such additions cannot be essential when they are added; and additions can later become essential as the system comes to depend on them as other changes accumulate. Given this, the ID argument from IC is susceptible to false positives: IC systems are not reliable indicators of “design” in the ID sense, since evolutionary mechanisms can produce them. In the next post in this series, we will examine other examples of IC systems and the evidence for their evolutionary origins.

For further reading:

  • Behe, M.J. Darwin’s Black Box: the Biochemical Challenge to Evolution. Free Press, New York, 1996.
  • Behe, M.J. The Edge of Evolution: the Search for the Limits of Darwinism. Free Press, New York, 2007.
  • Chen, S., Zhang, Y, and Long, M (2010). New genes in Drosophila quickly become essential. Science 330; 1682-1685.
  • Boltz, K, Ellis, L, and Carney, G (2007). Drosophila melanogaster p24 genes have developmental, tissue-specific, and sex-specific expression patterns and functions. Developmental Dynamics 236; 544-555.
  • Port, F, Hausmann, G, and Basler, K (2011). A genome-wide RNA interference screen uncovers two p24 proteins as regulators of Wingless secretion. EMBO reports 12; 1144 – 1152.
  • Beuchling, T, Chaudhary, V, Spirohn, K, Weiss, M, and Boutros, M (2011). p24 proteins are required for secretion of Wnt ligands. EMBO reports 12; 1265 – 1272.
  • Saleem, S, Schwedes, C, Ellis, L, Grady, S, Adams, R, Johnson, N, Whittington, J, and Carney, G (2012). Drosophila melanogaster p24 proteins have vital roles in development and reproduction. Mechanisms of Development (in press).

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. Dennis writes regularly for the BioLogos Forum about the biological evidence for evolution.

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Bilbo - #69997

May 18th 2012

Hi Dennis,

A few questions:

“1. Different defects are seen when the two genes are removed. While removing either gene usually results in the death of the fly, some rare flies do survive to adulthood. The survivors, however, have different defects: the loss of the Éclair gene results in female flies that cannot lay eggs, but loss of the p24-2 gene has no effect on egg laying at all.”

Could the fact that the p24-2 gene has no effect on egg laying indicate that the p24-2 gene has suffered a loss of function? 

“2.  Éclair and p24-2 are not always found in the same cell types during development. For example, p24-2 protein is not found in the ovaries of adult females, whereas Éclair protein is very abundant in this tissue. This difference likely explains why removing Éclair is so detrimental to laying eggs, but removing p24-2 is of no consequence at all for egg laying.”

Again, could the fact that p24-2 protein is not found in the ovaries of adult females indicate a loss of function by the p24-2 protein?

“3.  Éclair seems to share some functions with other p24 proteins that are less closely related to it than p24-2 is. For example, the “Basier” gene is found in all the same tissues in which Éclair is found. If a fly lacks Éclair, then it must have Basier (the flies all die if Basier is also removed). Similarly, when a fly lacks Basier, no loss of Éclair can be tolerated. These two genes work together and share their essential functions.”

You haven’t told us about the relationship between the Basier gene and p24-2, so it’s difficult to know what conclusion you are drawing here. 

“4.  One target “cargo” of Éclair has been identified - an important signaling protein called Wingless. The Wingless protein needs to be exported out of the cell in order to do its job, and without functional Éclair present, Wingless cannot make it from the ER to the Golgi, which it needs to do in order to be exported. The p24-2 protein, however, is completely dispensable for exporting Wingless. Thus p24-2 and Éclair are involved in transporting different cargo proteins. Éclair shares the function of exporting Wingless with another p24 family member (called Emp24), but not with its closer relative, p24-2.”

Again, could we interpret this as indicating that p24-2 has suffered a loss of function.

From the information that you have provided so far, it’s not clear that the p24-2 gene has resulted in a gain of function, especially of new pathways or machines.


dennis.venema - #69999

May 18th 2012

Hi Bilbo – thanks for the questions. My answers are below. This will likely spread across several comments due to space limitations.

1. Could the fact that the p24-2 gene has no effect on egg laying indicate that the p24-2 gene has suffered a loss of function? 

It’s possible, but that assumes that the nascent p24-2 gene was expressed (made into mRNA and translated into protein) in ovaries when the duplication happened. Another possibility is that the copied gene was never expressed in ovaries to begin with. The cell types that a given gene is expressed in depends on the non-coding DNA that surrounds the gene, and the copied version (p24-2) appears to have had different non-coding DNA from the start. In fact, it’s likely that it started out using the non-coding DNA of the neighboring gene Unc-115b, and continues to do so (at least in part) to this day. Even assuming that p24-2 had a function in ovaries at the beginning and lost this role, that is only one role/function. Proteins tend to have many roles/functions. 


dennis.venema - #70000

May 18th 2012

2. Again, could the fact that p24-2 protein is not found in the ovaries of adult females indicate a loss of function by the p24-2 protein?

See above – it assumes that p24-2 had a function in ovaries to begin with. 

 

3.  You haven’t told us about the relationship between the Basier gene and p24-2, so it’s difficult to know what conclusion you are drawing here. 

Sorry, I guess what seems obvious to me isn’t obvious to all. Recall that p24-2 is an essential gene – if you take it away, the flies die. If you take away Éclair, a small number of flies survive, since the function of Éclair can be covered by Basier (to a small extent). Even with normal amounts of Basier (or Éclair), removing p24-2 is lethal. So, the copied gene (p24-2) is more essential than its parent gene (in its modern-day form). This shows us that p24-2 has a new function that neither Basier nor Éclair can cover for.

 


dennis.venema - #70001

May 18th 2012

“4.  One target “cargo” of Éclair has been identified - an important signaling protein called Wingless. The Wingless protein needs to be exported out of the cell in order to do its job, and without functional Éclair present, Wingless cannot make it from the ER to the Golgi, which it needs to do in order to be exported.

The p24-2 protein, however, is completely dispensable for exporting Wingless. Thus p24-2 and Éclair are involved in transporting different cargo proteins. Éclair shares the function of exporting Wingless with another p24 family member (called Emp24), but not with its closer relative, p24-2.”

Again, could we interpret this as indicating that p24-2 has suffered a loss of function?

This also assumes that at the point of duplication, that p24-2 was capable of exporting Wingless. This is possible (and plausible, as long as p24-2 was expressed in the cell types where Wingless is made).  So, it may well be that p24-2 has lost the ability to export Wingless. Or, it may be the case that at the point of duplication p24-2 was not in the same cell types where Wingless is made, so it didn’t have that function from the start.

Either way, the point is that we know it is doing something essential, and that it does not have the same role as its parent gene. How could this be possible without it gaining a new function, even if it has lost others?


dennis.venema - #70002

May 18th 2012

From the information that you have provided so far, it’s not clear that the p24-2 gene has resulted in a gain of function, especially of new pathways or machines.

Don’t forget that all other Drosophila species don’t even have p24-2 at all, so the presence of p24-2 in D. melanogaster is a new pathway (genes in the p24 family don’t do their function in isolation, but as part of a large complex of proteins) and a new function of some sort. Proteins of this class shuttle other proteins around, and we know that whatever p24-2 is doing is now essential. The amino acid changes clustered together is very suggestive of a new protein-protein interaction site, which would make sense of the other lines of evidence.  


dennis.venema - #70003

May 18th 2012

Bilbo, the last point to make would be for you to consider Behe’s comments. The model he proposed for a new gene becoming essential was that the two genes have alterations that reduce their function, forcing them to share that function to compensate. Behe uses this speculative model to explain how the two genes can become  essential without “doing anything new.” 

Yet here with p24-2 and Eclair, we see that these two proteins are expressed in different places, interact with different cargo proteins, and one is absolutely essential (p24-2) and the other is partially compensated for when removed by other proteins (Basier, and likely Emp24).

Does this sound like it matches Behe’s speculation?


Bilbo - #70006

May 19th 2012

Hi Dennis,

You wrote:

“See above – it assumes that p24-2 had a function in ovaries to begin with.”

Given that p24-2 was originally a copy of Eclair, I would think that was a safe assumption.  The fact that it doesn’t have that function now would suggest that it either lost that function, or (thanks for pointing this out, since , as an armchair philosopher, I never would have thought of it) that it is not expressed in the ovaries.  But either way, this doesn’t show that p24-2 has a new function.

“Sorry, I guess what seems obvious to me isn’t obvious to all. Recall that p24-2 is an essential gene – if you take it away, the flies die.”

But compare this with what you wrote in the original post:

“While removing either gene usually results in the death of the fly, some rare flies do survive to adulthood.”

So now you appear to be saying that “some rare flies do survive” only when the Eclair gene is removed.  But when the p24-2 is removed, no flies survive?  Okay, now let’s go back and interpret the data.  Do all flies die when p24-2 is removed because p24-2 performs some new essential function?  Or has p24-2 taken over a function that Eclair used to perform?  Or is p24-2 expressed more, so that Eclair, even though it performs the same function as p24-2, performs it at a much lower level, so that as long as Basier is expressed, the fly survives?  But when both Eclair and Basier are removed, p24-2 isn’t able to compensate for both of them?  But when p24-2 is removed, Eclair and Basier aren’t able to compensate for it?   Again, the data isn’t telling us what we need to know: Is p24-2 actually performing a new function?

“The p24-2 protein, however, is completely dispensable for exporting Wingless. Thus p24-2 and Éclair are involved in transporting different cargo proteins.”

Or perhaps Eclair is involved in transporting other cargo, besides Wingless.  And this other cargo is also exported by p24-2.  Only p24-2 is expressed more than Eclair and exports more of this other cargo than Eclair.   It would help a lot if we identified what this other cargo was that p24-2 is involved in transporting.

“The amino acid changes clustered together is very suggestive of a new protein-protein interaction site, which would make sense of the other lines of evidence.”

From the little that I know, I agree that it is suggestive of a new protein-protein interaction site.  So let’s find out what that interaction site is.  Otherwise, I don’t think you’ve delivered the death-blow to Behe’s position, yet.



dennis.venema - #70007

May 19th 2012

Hi Bilbo,

DV: “Sorry, I guess what seems obvious to me isn’t obvious to all. Recall that p24-2 is an essential gene – if you take it away, the flies die.”

B: But compare this with what you wrote in the original post:

DV: “While removing either gene usually results in the death of the fly, some rare flies do survive to adulthood.”

B: So now you appear to be saying that “some rare flies do survive” only when the Eclair gene is removed.  But when the p24-2 is removed, no flies survive?  Okay, now let’s go back and interpret the data.  Do all flies die when p24-2 is removed because p24-2 performs some new essential function?  Or has p24-2 taken over a function that Eclair used to perform? 

Removing p24-2 pretty much kills all the flies, except for very rare survivors (in the one paper they all die, and in the other I think they observed only one survivor, if memory serves). Removing Éclair or Basier kills about 90% of the flies, so p24-2 is “more essential” than the other two essentials. In the wild, all three genes would be essential genes. I agree that it’s interesting to speculate what exactly p24-2 is doing, and how it got to be that way, but that’s a bit beside the point. Just how “new” the function of p24-2 is is something of a red herring, even though the evidence at present points to a new protein-protein interaction as part of its function. Remember, I’m critiquing Behe’s argument from IC.


dennis.venema - #70008

May 19th 2012

How do we tell if a system is IC? If we remove any part and the system stops functioning, the system is IC, according to Behe.

The argument from IC is not that such systems exist, but that such systems cannot be built by intermediate pathways that add components – they have to be “fully formed” from the start. Behe discusses, and dismisses, the intermediate pathway model in Darwin’s Black Box (see the first post in the Understanding Evolution series that deals with Irreducible Complexity, it’s all quoted).

In most Drosophila species, Basier and Éclair are present without p24-2, and Basier and Éclair have essential roles.

In Drosophila melanogaster, Basier, Éclair and p24-2 are present, and all three have essential roles. None can be removed without seriously compromising the system. Yet the evidence points convincingly that p24-2 is a recent addition to the system, that due to changes of some sort, has integrated into the system and become essential, through an intermediate path. As such, Behe cannot be confident that when he examines an IC system (under his definition) that it was not similarly produced by an intermediate pathway from an non-IC precursor system.

Recall too that the systems Behe commonly points to are ancient ones (such as the flagellum). This example is only 3 million years old or less. One would expect that the “new” functions and changes would be relatively modest. The point is that it shows that additions and modifications are possible, and that the additions can later become essential partners. The question for Behe, then, would be “what stops this process from accruing new proteins and functions over millions, or even billions of years? How can you be confident that systems you point to as IC did not in fact experience this process of addition in the past? How can you be sure that you’re not dealing with a false positive?”


dennis.venema - #70009

May 19th 2012

And, as we will see in an upcoming post, Behe’s answer to how we deal with this sort of thing is his proposed “Edge” of evolution. We’ll also see why biologists in general, and myself included, don’t think that his argument holds up. 


Bilbo - #70010

May 19th 2012

Hi Dennis,

You wrote:

“I agree that it’s interesting to speculate what exactly p24-2 is doing, and how it got to be that way, but that’s a bit beside the point. Just how “new” the function of p24-2 is is something of a red herring, even though the evidence at present points to a new protein-protein interaction as part of its function. Remember, I’m critiquing Behe’s argument from IC.”

I’m afraid I have to disagree with you.  Knowing exactly what new function p24-2 is performing is crucial to a sound critique of Behe’s IC.  Has a new pathway or machine evolved?  Or is p24-2 just filling a role that Eclair used to have?  I agree that it looks like p24-2 may have a new protein-protein interaction, but I think we need to know for sure what it is. 

When discussing Behe’s Edge, I hope you keep in mind his comment on page 157:

“The conclusion from Chapter 7—that the development of two new intracellular protein-protein binding sites at the same time is beyond Darwinian reach—leaves open, at least as a formal possibility, that some multiprotein structures (at least ones that aren’t irreducibly complex, in the sense defined in Darwin’s Black Box) might be built by adding one protein at a time, each of which is an improvement.”


dennis.venema - #70011

May 19th 2012

Bilbo, is the function of p24-2, Eclair, and Basier in D. melanogaster IC, according to Behe’s definition in DBB?

If not, why not?


dennis.venema - #70012

May 19th 2012

And yes, I’ll be dealing with that comment from EoE. They key issue is “at the same time.” If the sites don’t need to be present “at the same time” but can arise through serial changes over time, then Behe hasn’t found an edge to what evolution can do. 


melanogaster - #70017

May 20th 2012

Bilbo:
“Knowing exactly what new function p24-2 is performing is crucial to a sound critique of Behe’s IC.”

What? Wouldn’t it be BEHE’S crucial responsibility to know exactly before promoting IC? Wouldn’t it be YOUR responsibility to know before critiquing Dennis’s critique?

Come on, Bilbo, how many cases did Behe use? Don’t forget that one of them (HIV) has been unequivocally been shown to be based on a false claim.


Bilbo - #70013

May 19th 2012

Dennis, you asked,

“Bilbo, is the function of p24-2, Eclair, and Basier in D. melanogaster IC, according to Behe’s definition in DBB?”

If they are in single multi-part systems, with well-matched, interacting parts, where the removal of a single part causes the system to cease functioning, I would say yes.  (In DBB, Behe was careful to exclude metabolic pathways that don’t require interaction between proteins.  So I was a little surprised to see him include “pathways” in his reply to Coyne.  Was he being careless?)

I agree with your second comment.


dennis.venema - #70014

May 19th 2012

Hi Bilbo,

Thanks for your reply. Just so I am clear, are you not convinced that p24-2  is part of a mutli-part system with well-matched, interacting parts?

Glad to see you’re in agreement with the second point - we’ll cover the evidence that binding sites can arise bit by bit in future posts. I’ll look forward to your questions and comments there - you’ve asked some good questions here. Thanks. 

Dennis 


Bilbo - #70015

May 19th 2012

I’m not convinced that p24-2 is part of a new multi-protein complex or new pathway.  I’m glad you appreciate my questions and comments.  I appreciate your efforts in taking Behe’s IC head-on.


dennis.venema - #70035

May 21st 2012

Hi Bilbo, 

Do you have a precise definition of “new” that you’re working with? Since much turns on what you mean by “new” I’m wondering if you could describe what you mean by it. Would p24-2 binding a protein that neither Eclair nor Basier binds to qualify as “new”, for example? 

Dennis 


Bilbo - #70023

May 21st 2012

Hi Melanogaster (mind if I shorten it to Melano?),

You wrote:

“What? Wouldn’t it be BEHE’S crucial responsibility to know exactly before promoting IC? Wouldn’t it be YOUR responsibility to know before critiquing Dennis’s critique?”

Behe has offered a challenge to Darwinian evolutionists:  explain how IC systems evolved through Darwinian processes or admit that there’s a serious flaw in Darwinian theory.  Dennis seems to be claiming that the new gene p24-2 is involved in a new IC system.  Okay, perhaps it is.  And if it is, then I think that would be a good counter-challenge to Behe.  But before we accept Dennis’s claim, shouldn’t we know in what new IC system p24-2 is involved?  What if it turns out that there is no new IC system?  What if it turns out that p24-2 is just replacing what Eclair used to do in the same old system?  If we found that out, I don’t think it would be a good counter-challenge to Behe’s argument.

“Come on, Bilbo, how many cases did Behe use? Don’t forget that one of them (HIV) has been unequivocally been shown to be based on a false claim.”

I think Behe has proposed about half a dozen cases of IC.  In the case of HIV, Behe wasn’t using HIV as a case of an IC system.  Behe was arguing about the difficulty of producing new proteins.  This was part of his quest to determine the “edge” of evolution—what can be explained by natural selection acting upon random mutations, and what can’t be explained that way.  Eventually, in his book, Behe came to the conclusion ...(drum roll, please)...that Darwinian evolution can produce new systems, as long as it can happen one protein at a time.  If it takes two or more proteins being produced simultaneously to produce a new system,
then this would be beyond the reach (or edge) of Darwinian evolution.

So yes, even Behe admitted that he was mistaken, and that HIV had produced a new protein.  The question is, did this result in a new system, such as a new molecular machine or pathway?  And given that the mutation rate in HIV is 10,000 times higher than in living organisms, can we legitemately extrapolate from what HIV evolved to what living organisms can evolve?


melanogaster - #70056

May 22nd 2012

“Behe has offered a challenge to Darwinian evolutionists: ”

Please, Bilbo, stop right there. You know that’s not true. Behe wrote a book aimed entirely at laypeople to create such an impression. If Behe was really a part of the scientific enterprise, he’d be offering his challenge by generating and publishing data by working in his lab.

Behe was trained as an empiricist, not a theoretician. If you want to argue that he has any business limiting himself to theory, you need to explain why Behe doesn’t read the relevant primary literature. He testified under oath that he does not, even for an example that he chose to emphasize!

“…Dennis seems to be claiming that the new gene p24-2 is involved in a new IC system.”

Bilbo, the issue is not what Dennis is claiming. The issue is the data that Dennis is pointing out to you. Now, I would give you 1000:1 odds that Behe has never read the papers that Dennis is citing here. Do you agree or disagree?

“…Eventually, in his book, Behe came to the conclusion ...(drum roll, please)...that Darwinian evolution can produce new systems, as long as it can happen one protein at a time.”

But was his conclusion based on an understanding of the data?

“So yes, even Behe admitted that he was mistaken, and that HIV had produced a new protein.”

How long did it take him to admit that from the time it was pointed out to him? More importantly, why would something so basic need to be pointed out to someone who bases his conclusion on so few cases?

“The question is, did this result in a new system, such as a new molecular machine or pathway?”

The data say yes.

“And given that the mutation rate in HIV is 10,000 times higher than in living organisms, can we legitemately extrapolate from what HIV evolved to what living organisms can evolve?”

Absolutely, because we are capable of doing basic math. Are you?


Bilbo - #70038

May 21st 2012

Dennis,  you wrote:

“Do you have a precise definition of “new” that you’re working with? Since much turns on what you mean by “new” I’m wondering if you could describe what you mean by it. Would p24-2 binding a protein that neither Eclair nor Basier binds to qualify as “new”, for example? ”

I was thinking of “new” in conjunction with “function,”  as in new molecular machine or new pathway.  But let’s say that p24-2 binds to a protein that neither Eclair nor Basier bind to, but no new function results and it’s considered a neutral mutation.  I think this would be a gray area, where we might end up arguing for or against Behe’s position.  Again, let’s say that p24-2 binds to a different site of a protein that is in the same complex as Eclair, but because of this new binding site, the complex accomplishes the function more effeciently and is selected for, and eventually Eclair is completely replaced by p24-2.  Should we say that a new IC system has evolved?  Or just that the old IC system has become more efficient?  I would more likely choose the second option.  Does this help?


marklynn.buchanan - #70040

May 21st 2012

Dennis,

I really appreciate your articles.

When I first read this latest article I was disappointed - I was expecting something easy to understand and fairly simple. Alas evolutionary biology is very complex, particularly for the layman, and takes some effort to understand.

I agree with Bilbo that there ‘could’ be various interpretations of the p24-2 data - Behe’s being one of them. The likeliest however is that p24-2 is something ‘new’ and that it has evolved into an essential role as part of an interconnected complex system.

Following on from Bilbo’s latest comment (# 70038) it seems there could be 3 different options for the function of p24-2:

  1. It does perform some sort of duplicate function related to Eclair and is a straight forward copy/modify that would fit into Behe’s framework.
  2. It performs something independent of from Eclair’s function(s) and is unrelated to other systems (although obviously very similar to other systems).
  3. It is an essential part of a complex system independent of Eclair’s various functions.

1 seems unlikely because of the evidence presented. However, even if the new p24-2 does fit into Behe’s IC framework somehow the fact that the inter-dependencies between the two genes would mean that there is a very different IC system now than there was before.

2 or 3 would imply something truly ‘new’.

Mark Buchanan


Bilbo - #70058

May 22nd 2012

Hi Melano,

You wrote:

“Please, Bilbo, stop right there. You know that’s not true. Behe wrote a book aimed entirely at laypeople to create such an impression. If Behe was really a part of the scientific enterprise, he’d be offering his challenge by generating and publishing data by working in his lab.”

What sort of data did you have in mind?

“... you need to explain why Behe doesn’t read the relevant primary literature. He testified under oath that he does not, even for an example that he chose to emphasize!”

Did he say that he didn’t read it or that it wasn’t relevant to his point?

“Bilbo, the issue is not what Dennis is claiming. The issue is the data that Dennis is pointing out to you. Now, I would give you 1000:1 odds that Behe has never read the papers that Dennis is citing here. Do you agree or disagree?”

You’ve made three statements, so I’m not sure which one you mean, but I happen to disagree with all of them.  I don’t want to cause you financial hardship, so I’ll bet you $0.001.  That way, if I win I think you would owe me $1.00, which you may donate to the charity of your choice in my name.

Bilbo: “…Eventually, in his book, Behe came to the conclusion ...(drum roll, please)...that Darwinian evolution can produce new systems, as long as it can happen one protein at a time.”

Melano: “But was his conclusion based on an understanding of the data?”

The “drum roll, please” should have been a good hint that his conclusion isn’t really all that controversial.

“How long did it take him to admit that from the time it was pointed out to him?”

I dunno.  I’ll guess from the time he finally read Abbey’s incredibly disrespectful essay, until the time he checked the literature?

“More importantly, why would something so basic need to be pointed out to someone who bases his conclusion on so few cases?”

My guess is that the HIV data was published after EoE was published.

“The data say yes [a new system was created in HIV].

Really?  What was it?

Bilbo: “And given that the mutation rate in HIV is 10,000 times higher than in living organisms, can we legitemately extrapolate from what HIV evolved to what living organisms can evolve?”

Melano: “Absolutely, because we are capable of doing basic math. Are you?”

Sometimes.  I think I know the difference between 10,000 and 1.

Reply to this comment


melanogaster - #70130

May 26th 2012

“What sort of data did you have in mind?”

The sort of data that Abbie Smith cited so impolitely.

“Did he say that he didn’t read it or that it wasn’t relevant to his point?”

Both. Moreover, how could possibly he know that something isn’t relevant if he hasn’t read it?

““The “drum roll, please” should have been a good hint that his conclusion isn’t really all that controversial.”

According to someone who frames science as claims and ignores the data?

Why not answer the question? Was it based on an understanding of the data?

“I dunno.  I’ll guess from the time he finally read Abbey’s incredibly disrespectful essay, …”

Why is the respectfulness of the essay an issue if Behe’s got a case based on the data?

“…until the time he checked the literature?”

Why wouldn’t he have checked it thoroughly BEFORE writing a book on the subject? 

“My guess is that the HIV data was published after EoE was published.”

Reality begs to differ. Wanna guess the number of years by which your guess is wrong?

“Really?  What was it?”

A viroporin. Why are you so aggressively categorizing Abbie as disrespectful if you have no familiarity with the content of her writing, Bilbo?

Bilbo: “And given that the mutation rate in HIV is 10,000 times higher than in living organisms, can we legitemately extrapolate from what HIV evolved to what living organisms can evolve?”

Melano: “Absolutely, because we are capable of doing basic math. Are you?”

Sometimes.  I think I know the difference between 10,000 and 1.

So how long would it take a human population to evolve past Behe’s vaunted edge and produce a new protein-protein binding site based on HIV?

And how long does it take an individual human—for example, you—to evolve a new protein-protein binding site by no mechanisms other than genetic variation and selection?

When was the last time you had a cold or flu, Bilbo?


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